Myocardial stunning: do we know the mechanism?
In response to the challenge of the title of this article, it is clear that we do know the principal players involved in myocardial stunning. We know that: approximately 80-85% of stunning can be attributed to free radicals the principal targets for free radical damage are the proteins involved in E-C coupling the action potential and the Ca transient remain largely intact in the stunned myocardium and thus the principal lesion in stunned hearts is at the level of the myofilaments myofilament damage can be induced either directly by free radicals or indirectly via Ca overload-induced activation of proteases which degrade myofilament proteins Ca overload and free radicals are likely to interact to promote stunning the 15-20% of stunning which is not directly attributable to free radicals is likely to reflect damage mediated by Ca overload this free radical-independent Ca overload is principally mediated via the activation of Na/Ca exchange secondary to the activation of Na/H exchange a principal player in reperfusion-induced Ca overload is the recovery of intracellular Na which may be compromised by both damage to the Na/K pump and the physical translocation of the pump away from the sarcolemmal membrane.
Shattock
M J
MJ
Rayne Institute St. Thomas' Hospital London. m.shattock@umds.ac.uk
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D009200:Myocardial Contraction; D017682:Myocardial Stunning / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology
D000975:Antioxidants; D005609:Free Radicals; D002118:Calcium